Multiple Sclerosis

Multiple sclerosis (MS), an autoimmune disease of the central nervous system, progressively destroys axonal myelin sheaths and oligodendrocytes. Symptoms primarily result from the loss of myelin and accompanying inflammation. This disease typically progresses with acute attacks (relapses) characterized by T cell invasion and inflammation resulting in white matter lesions, with a period of remission where neuronal cells can recover. One central focus of MS research is the use of microarray analyses of white matter lesions from postmortem patients to identify novel genes that may explain MS mechanisms and potentially yield new therapeutic targets. Genes mediating MS progression include cytokines and chemokines as well as inflammatory and immune response genes. In addition, genes with changes in expression that correlate across multiple microarray expression analyses can potentially enabled the identification of novel cellular functions involved in this disease, such as cell adhesion, cellular stress, and apoptosis. ...

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Multiple sclerosis (MS), an autoimmune disease of the central nervous system, progressively destroys axonal myelin sheaths and oligodendrocytes. Symptoms primarily result from the loss of myelin and accompanying inflammation. This disease typically progresses with acute attacks (relapses) characterized by T cell invasion and inflammation resulting in white matter lesions, with a period of remission where neuronal cells can recover. One central focus of MS research is the use of microarray analyses of white matter lesions from postmortem patients to identify novel genes that may explain MS mechanisms and potentially yield new therapeutic targets. Genes mediating MS progression include cytokines and chemokines as well as inflammatory and immune response genes. In addition, genes with changes in expression that correlate across multiple microarray expression analyses can potentially enabled the identification of novel cellular functions involved in this disease, such as cell adhesion, cellular stress, and apoptosis.